Haemobartonella felis and H. canis are bacteria that previously were thought to be rickettsias, based on their appearance and behaviour in cat and dog blood. However, they have been reevaluated phylogenetically and placed as a haemocytic clade within the family Mycoplasmataceae. 'Haemoplasma' is considered a trivial name for this group. The classification of haemoplasmas in the Mollicutes is reflected in the ultrastructure: there is a plasma membrane, no cell wall and no internal membranous structures. As with other mycoplasmas, the cell requires cholesterol from the environment for incorporation into the plasma membrane. There is a virulent large feline parasite which has been renamed Mycoplasma haemofelis and a small form with low pathogenicity named M. haemominutum. There are at least two canine species: a large form designated M. haemocanis and a small form M. haemoparvum, which is more closely related to the small feline form than the large canine form. The organisms are technically gram-negative. They attach by filamentous bridges to the surface of red blood cells. The mode(s) of transmission among animals are not known.

In dogs, haemobartonellosis occurs primarily only in splenectomized or immunosuppressed dogs and is characterized as an acute anaemia with the organism easily visualized on the red cells. Infected cats often are completely asymptomatic, especially if infected with the small form, or they may develop acute or cyclic anaemia (feline infectious anaemia or FIA). Signs of disease occur after IgG is produced (at least 10 days after exposure), at which time the spleen attempts to remove opsonised bacteria and leaves behind spherocytes with high osmotic fragility (also Coombs'-positive). Clinical signs associated with severe haemobartonellosis include pallor, dyspnoea with open-mouth breathing, weakness and fever. After a single episode, there may ensue a series of infection cycles, consisting of periods of latency and recrudescence lasting 2-4 months. There may be 3-9 parasitaemic episodes with 3-11 days between peaks of parasitaemia. These recrudescent attacks become increasingly less severe (in terms of percentage parasitism, reductions in packed cell volume (PCV) and clinical signs) with each attack: only the first one or two attacks may be clinically apparent. It is also common for cats to become healthy carriers. The reservoir within the body in carrier cats in unknown, but M. haemofelis organisms can occasionally be visualized within splenic and pulmonary macrophages. If untreated, the mortality rate for clinical FIA may exceed 33%.

FIA tends to be more severe in cats with other conditions including stress, pregnancy, neoplasia or other infection. In particular feline leukaemia virus (FeLV) infection is well described for potentiating haemobartonellosis, especially the small form. Feline immunodeficiency virus (FIV) is not statistically associated with severe FIA. Cats with concurrent haemobartonellosis and FeLV are usually much sicker, with more profound and refractory anaemia, than cats with FIA alone. Cats with both FeLV and M. haemofelis or M. haem ominutum infection may have haematological changes both from the effects of FIA as well as the typical myeloproliferative disease, aplastic anaemia, or various dyshaemopoietic disorders of FeLV.

Haemobartonellosis is diagnosed on complete blood count (CBC) or with polymerase chain reaction (PCR). There may be frank blood loss (macrocytic anaemia with reticulocytosis), although commonly the anaemia may be normocytic normochromic. The PCV may decline to 15% or lower. Clinical signs occur once the PCV falls below about 20% by which time about 50% cats have large numbers of parasitised erythrocytes in circulation. Nucleated red blood cells may occur in FIA, reflecting hypoxic trauma to the bone marrow. Leucocyte responses in FIA are variable, including leucopenia with toxic neutrophils or leucocytosis. Haemobartonella organisms can be stained with Wright- Giemsa or new methylene blue stains and appear as dark blue or gram-positive variably shaped 0.3-0.8 µm bodies on the surface of feline erythrocytes. The fraction of erythrocytes that is parasitised is variable, as high as 95% in acutely ill cats, with 10 or more organisms observed in pairs or chains on the surface of erythrocytes. The parasites may be confused with Howell-Jolly bodies, but H-J bodies are at least twice as large as the M. haemofelis organisms and non-refractile. Several different Haemobartonella-specific PCR tests are available, targeting the 16S rRNA subunit gene for the different species. PCR for FIA is generally more sensitive than other methods of diagnosis, e.g., haematology.

Because haemoplasmas lack cell walls, penicillin and cephalosporin-class drugs are ineffective. The treatment of choice is one of the tetracycline class drugs (tetracycline, oxytetracycline or doxycycline). Oxytetracycline is convenient because it can be given less frequently but can cause pain on administration and local reactions at the site of injection. In anaemic cats treated with tetracyclines, clinical signs may resolve within 24 hours and results of PCR tests may become negative during treatment, although the development of negative results can occur a variable length of time following the start of treatment.

Some cases of FIA are refractory to tetracycline. Although controlled studies are generally lacking, possible alternative treatments for FIA include thiacetarsamide, chlorpromazine, chloramphenicol, and a combination of spiramycin, metronidazole and chloramphenicol. More recent suggestions include enrofloxacin, or marbofloxacin which may help avoid some retinal complications of enrofloxacin. These drugs will successfully improve the cat's clinical condition and lead to increased PCV but do not necessarily eliminate 'haemoplasma' DNA.

In addition to antibiotic therapy, supportive therapy may be necessary to prevent severe hypoxia and death. Corticosteroids (e.g., prednisolone at 1-2 mg/kg orally daily for the first 7-14 days) may be used to prevent the immune-mediated erythrophagocytosis of infected erythrocytes. Blood transfusion is frequently necessary, but transfused cells are very susceptible to parasitism and may need to be given repeatedly. An alternative might be transfusion with Oxyglobin, a polymerised bovine haemoglobin product licensed for use in anaemic dogs. The epidemiology of haemobartonellosis is poorly understood. All four haemoplasma species of dogs and cats have been detected in North America and Europe. Animals at increased risk of haemobartonellosis are older, male, indoor-outdoor and infested with fleas. The incidence of FIA increases with age with a peak incidence from 4-8 years. Infection with M. haemofelis appears to be seasonal. Suggested routes of infection are in utero or lactogenic, iatrogenic, possibly oral, and haematophagous arthropod. In utero or lactogenic infection is suggested by detection of haemobartonellosis in very young kittens. Blood-sucking arthropods such as fleas might be natural vectors, although many cases have been identified in Salt Lake City, Utah, in the absence of fleas. Canine haemoplasmas appear to be transmitted via the brown dog tick Rhipicephalus sanguineus.